Smoking accounts for more than a third of cases of the most severe and common form of rheumatoid arthritis, indicates research published online in the Annals of the Rheumatic Diseases. And it accounts for more than half of cases in people who are genetically susceptible to development of the disease, finds the study.
The researchers base their findings on more than 1,200 people with rheumatoid arthritis and 871 people matched for age and sex, but free of the disease. The patients came from 19 health clinics in south and central Sweden, while their healthy peers were randomly selected from the population register. All the participants were aged between 18 and 70. They were quizzed about their smoking habits and grouped into three categories, depending on how long they had smoked. Blood samples were taken to assess all the participants' genetic profile for susceptibility to rheumatoid arthritis and to gauge the severity of their disease, as indicated by their antibody levels.
More than half of those with rheumatoid arthritis (61%) had the most severe form of the disease, which is also the most common form, as judged by testing positive for anticitrullinated protein/peptide antibody (ACPA). Those who were the heaviest smokers – 20 cigarettes a day for at least 20 years – were more than 2.5 times as likely to test positive for ACPA. The risk fell for ex-smokers, the longer they had given up smoking. But among the heaviest smokers, the risk was still relatively high, even after 20 years of not having smoked.
Based on these figures, the researchers calculated that smoking accounted for 35% of ACPA positive cases, and one in five cases of rheumatoid arthritis, overall. Although this risk is not as high as for lung cancer, where smoking accounts for 90% of cases, it is similar to that for coronary artery heart disease, say the authors. Among those with genetic susceptibility to the disease, and who tested positive for ACPA, smoking accounted for more than half the cases (55%). Those who smoked the most had the highest risk.
The authors point out that several other environmental factors may contribute to an increased risk of rheumatoid arthritis, including air pollutants and hormonal factors. But they suggest that their findings are sufficient to prompt those with a family history of rheumatoid arthritis to be advised to give up smoking.
NAFLD is the most common cause of liver disease worldwide and research suggests the number of cases will climb given an increasing trend toward higher fat diets, obesity, decreased physical activity, and a rise in diabetes. Past studies indicate that more than 30 million Americans have NAFLD and approximately 8 million may have nonalcoholic steatohepatitis (NASH).
In the first study, Ramón Bataller, M.D., and colleagues from the Hospital Clínic in Barcelona, Spain investigated the effects of cigarette smoking (CS) in obese rats. Rats were divided into 4 groups (n=12 per group): obese smokers, obese non-smokers, control smokers and control non-smokers. Smoker rats were exposed to 2 cigarettes/day, 5 days/week for 4 weeks. Researchers found that obese rats exposed to CS showed a significant increase in ALT serum levels (indicating liver disease), while this effect was not observed in control rats.
“Our results show that CS causes oxidative stress and worsens the severity of NAFLD in obese rats,” said Dr. Bataller. “Further studies should investigate longer exposures to CS, and assess whether this finding also occurs in patients with obesity and NAFLD.”
In her editorial, also published in Hepatology this month, Claudia Zein, M.D., from the Cleveland Clinic, noted that “the importance of these results is that taken together with other experimental and clinical data, they support that cigarette smoking appears to aggravate liver injury in patients with liver disease.” Dr. Zein added, “Studies characterizing the effects of cigarette smoking in human NAFLD will be crucial because of the vast number of patients that may benefit from modification of this risk factor.”
Additionally, prior studies suggest an over consumption of high fructose corn syrup (HFCS), primarily in the form of soft-drinks, have contributed to weight gain and the rise in obesity, particularly in children and adolescents. Table sugar (sucrose) and HFCS are the two major dietary sources of fructose. Over the past 40 years, consumption of dietary fructose has increased 1,000% according to Bray et al, and doctors believe it to be a major cause of NAFLD.
Researchers from Duke University studied 341 adults enrolled in the NASH Clinical Research Network who responded to a Block food questionnaire within 3 months of a liver biopsy. Fructose consumption was estimated conservatively by including that found in beverages, which accounts for 50% of dietary fructose intake. Results showed that 27.9% of participants consumed at least 1 fructose-containing beverage per day, 52.5% had 1 to 6 beverages with fructose per week, and 19.7% drank no beverages with fructose.
“In patients with NAFLD, daily fructose ingestion was associated with reduced fatty liver (steatosis), but we found increased fibrosis,” noted Manal Abdelmalek, M.D., M.P.H, and lead author of the study. “Further dietary intervention studies are needed to evaluate whether a low-fructose diet improves metabolic disturbances associated with NAFLD and improves patient outcomes for those at risk of disease progression,” concluded Dr. Abdelmalek.
A second fructose study led by Ling-Dong Kong, M.D., from Nanjing University in China investigated the effects of curcumin on fructose-induced hypertriglyceridemia and fatty liver in rats. Curcumin, a compound derived from turmeric (curcuma root), is sold as an herbal supplement and is believed to have anti-inflammatory, anti-tumor, and anti-viral properties. Researchers observed a hyperactivity of hepatic protein tyrosine phosphatase 1B (PTP1B), which is associated with defective insulin and leptin signaling, in fructose-fed rats.
For the first time this study demonstrated that curcumin inhibited hepatic PTP1B expression and activity in fructose-fed rats. “Our results provide novel insights into the potential therapeutic mechanisms of curcumin on fructose-induced hepatic steatosis associated with insulin and leptin resistance,” said Dr. Kong.
These studies indicate modifying risks such as smoking and fructose consumption offer potential benefits for those with liver diseases. Further studies are needed to explore these benefits in preventing the progression of liver disease.
Ms. Agler and colleagues reviewed data compiled by the Women's Health Study, a multi-year, long-term effort ending in 2004 that focused on the effects of aspirin and vitamin E in the prevention of cardiovascular disease and cancer in nearly 40,000 women aged 45 years and older. Study participants were randomized to receive either 600 mg of vitamin E or a placebo every other day during the course of the research.
Although fewer women taking vitamin E developed COPD, Ms. Agler noted the supplements appeared to have no effect on asthma, and women taking vitamin E supplements were diagnosed with asthma at about the same rate as women taking placebo pills. Importantly, Ms. Agler noted the decreased risk of COPD in women who were given vitamin E was the same for smokers as for non-smokers.
Ms. Agler said further research will explore the way vitamin E affects the lung tissue and function, and will assess the effects of vitamin E supplements on lung diseases in men. “If results of this study are borne out by further research, clinicians may recommend that women take vitamin E supplements to prevent COPD,” Ms. Agler noted. “Remember that vitamin E supplements are known to have detrimental effects in some people; for example vitamin E supplementation increased risk of congestive heart failure in cardiovascular disease patients. Broader recommendations would need to balance both benefits and risks. “